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首页> 外文期刊>Mechanisms of Development >Reduction of Lobe leads to TORC1 hypoactivation that induces ectopic Jak/STAT signaling to impair Drosophila eye development
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Reduction of Lobe leads to TORC1 hypoactivation that induces ectopic Jak/STAT signaling to impair Drosophila eye development

机译：肺叶的减少导致TORC1激活不足，从而诱导异位Jak / STAT信号传导，从而削弱果蝇眼的发育

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The TOR and Jak/STAT signal pathways are highly conserved from Drosophila to mammals, but it is unclear whether they interact during development. The proline-rich Akt substrate of 40 kDa (PRAS40) mediates the TOR signal pathway through regulation of TORC1 activity, but its functions in TORC1 proved in cultured cells are controversial. The Drosophila gene Lobe (L) encodes the PRAS40 ortholog required for eye cell survival. L mutants exhibit apoptosis and eye-reduction phenotypes. It is unknown whether L regulates eye development via regulation of TORC1 activity. We found that reducing the L level, by hypomorphic L mutation or heterozygosity of the null L mutation, resulted in ectopic expression of unpaired (upd), which is known to act through the Jak/STAT signal pathway to promote proliferation during eye development. Unexpectedly, when L was reduced, decreasing Jak/STAT restored the eye size, whereas increasing Jak/STAT prevented eye formation. We found that ectopic Jak/STAT signaling and apoptosis are mutually dependent in L mutants, indicating that L reduction makes Jak/STAT signaling harmful to eye development. In addition, our genetic data suggest that TORC1 signaling is downregulated upon L reduction, supporting the idea that L regulates eye development through regulation of TORC1 activity. Similar to L reduction, decreasing TORC1 signaling by dTOR overexpression results in ectopic upd expression and apoptosis. A novel finding from our data is that dysregulated TORC1 signaling regulates the expression of upd and the function of the Jak/STAT signal pathway in Drosophila eye development.
机译：TOR和Jak / STAT信号通路从果蝇到哺乳动物均高度保守，但尚不清楚它们在发育过程中是否相互作用。 40 kDa的富含脯氨酸的Akt底物（PRAS40）通过调节TORC1活性来介导TOR信号通路，但在培养细胞中证明其在TORC1中的功能尚存争议。果蝇基因Lobe（L）编码了眼细胞存活所需的PRAS40直向同源物。 L突变体表现出凋亡和减少眼睛的表型。尚不清楚L是否通过调节TORC1活性来调节眼睛发育。我们发现通过亚型L突变或无效L突变的杂合性降低L水平会导致未配对的异位表达（upd），已知其通过Jak / STAT信号途径起作用，以促进眼发育过程中的增殖。出乎意料的是，当L减小时，减小的Jak / STAT恢复了眼睛的大小，而增大的Jak / STAT阻止了眼睛的形成。我们发现异位Jak / STAT信号和细胞凋亡在L突变体中是相互依赖的，这表明L的减少使Jak​​ / STAT信号对眼睛发育有害。另外，我们的遗传数据表明，L减少时，TORC1信号会下调，这支持L通过调节TORC1活性来调节眼睛发育的观点。与L减少类似，dTOR过表达减少TORC1信号传导会导致异位上调表达和凋亡。从我们的数据中发现的一个新发现是，果蝇眼发育中失调的TORC1信号传导调节了upd的表达以及Jak / STAT信号通路的功能。

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